Introduction Left ventricular assist device (LVAD) has emerged as an effective treatment of end-stage heart failure either as bridge to transplant or destination therapy. However, the need for anticoagulation with LVAD comes with the trade-off of increased bleeding risk and worsening anemia requiring blood transfusions. We describe a case of acute hemorrhagic shock in a Jehovah's Witness with a HeartMate 3 (HM3) - LVAD successfully treated without any transfusion of blood products Case A 65-year-old African American Jehovah's Witness male with a three months history of HM3 implantation for end-stage non-ischemic cardiomyopathy presented to the hospital for loss of consciousness, melanotic stool, hypotension and hemorrhagic shock. Initial laboratory included an elevated INR of 5.4 and hemoglobin of 5.4 g/dL. The LVAD remained in good function without low flow alarms at a speed of 4900 rpm and a SBP of 40mmHg. Patient's hypotension and decompensation was attributed to his acute blood loss anemia, however, given his religious beliefs, transfusion of blood products was not an option. As a result, the patient was intubated and resuscitated with IV iron, colloids and darbepoetin alfa for RBC stimulation in addition to inotropes and pressor support. Gastroenterology declined urgent endoscopic procedure due to the hemodynamic instability of this case. The patient's hemoglobin further declined to 2.4 g/dL with persistent, refractory shock. Only after an increase in LVAD speed from 4900 rpm to 5600 rpm cardiac output and overall hemodynamic status improved to MAP of 70 mmHg allowing de-escalation of inotropes and pressors. Over the next two weeks, INR corrected, bleeding subsided, and the patient was extubated without any neurological deficits or signs of mesenteric ischemia. His hemoglobin trended up to > 8 g/dL by discharge. Conclusion Bleeding is common in heart failure patients with LVADs. Blood transfusion, at times, can provide a simple and quick life-saving resolution to this problem. The severity of anemia in our case without administration of any blood products is usually not consistent with life. Our case highlights a potential role of augmenting LVAD support to maintain cardiac output in patients presenting with hypovolemic, hemorrhagic shock as a bridge to recovery of endogenous RBC mass regeneration with IV iron and darbepoetin alfa without the need of foreign blood products. Future studies are necessary to determine whether LVAD optimization is sufficient to avoid blood products and preventing the risk of sensitization BTT LVAD patients against potential future heart transplant offers.